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dc.contributor.authorLi, Wenhui
dc.contributor.authorGreenough, Thomas C.
dc.contributor.authorMoore, Michael J.
dc.contributor.authorVasilieva, Natalya
dc.contributor.authorSomasundaran, Mohan
dc.contributor.authorSullivan, John L.
dc.contributor.authorFarzan, Michael
dc.contributor.authorChoe, Hyeryun
dc.date2022-08-11T08:10:12.000
dc.date.accessioned2022-08-23T16:58:52Z
dc.date.available2022-08-23T16:58:52Z
dc.date.issued2004-10-01
dc.date.submitted2012-05-01
dc.identifier.citationJ Virol. 2004 Oct;78(20):11429-33. <a href="http://dx.doi.org/10.1128/JVI.78.20.11429-11433.2004">Link to article on publisher's site</a>
dc.identifier.issn0022-538X (Linking)
dc.identifier.doi10.1128/JVI.78.20.11429-11433.2004
dc.identifier.pmid15452268
dc.identifier.urihttp://hdl.handle.net/20.500.14038/43459
dc.description.abstractReplication of viruses in species other than their natural hosts is frequently limited by entry and postentry barriers. The coronavirus that causes severe acute respiratory syndrome (SARS-CoV) utilizes the receptor angiotensin-converting enzyme 2 (ACE2) to infect cells. Here we compare human, mouse, and rat ACE2 molecules for their ability to serve as receptors for SARS-CoV. We found that, compared to human ACE2, murine ACE2 less efficiently bound the S1 domain of SARS-CoV and supported less-efficient S protein-mediated infection. Rat ACE2 was even less efficient, at near background levels for both activities. Murine 3T3 cells expressing human ACE2 supported SARS-CoV replication, whereas replication was less than 10% as efficient in the same cells expressing murine ACE2. These data imply that a mouse transgenically expressing human ACE2 may be a useful animal model of SARS.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=15452268&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC521845/pdf/0880-04.pdf
dc.subject3T3 Cells
dc.subjectAnimals
dc.subjectCell Line
dc.subjectEndopeptidases
dc.subjectHumans
dc.subjectMice
dc.subjectPeptidyl-Dipeptidase A
dc.subjectRats
dc.subjectSARS Virus
dc.subjectSevere Acute Respiratory Syndrome
dc.subject*Virus Replication
dc.subjectImmunology and Infectious Disease
dc.subjectPediatrics
dc.titleEfficient replication of severe acute respiratory syndrome coronavirus in mouse cells is limited by murine angiotensin-converting enzyme 2
dc.typeJournal Article
dc.source.journaltitleJournal of virology
dc.source.volume78
dc.source.issue20
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/peds_immunology/41
dc.identifier.contextkey2814371
html.description.abstract<p>Replication of viruses in species other than their natural hosts is frequently limited by entry and postentry barriers. The coronavirus that causes severe acute respiratory syndrome (SARS-CoV) utilizes the receptor angiotensin-converting enzyme 2 (ACE2) to infect cells. Here we compare human, mouse, and rat ACE2 molecules for their ability to serve as receptors for SARS-CoV. We found that, compared to human ACE2, murine ACE2 less efficiently bound the S1 domain of SARS-CoV and supported less-efficient S protein-mediated infection. Rat ACE2 was even less efficient, at near background levels for both activities. Murine 3T3 cells expressing human ACE2 supported SARS-CoV replication, whereas replication was less than 10% as efficient in the same cells expressing murine ACE2. These data imply that a mouse transgenically expressing human ACE2 may be a useful animal model of SARS.</p>
dc.identifier.submissionpathpeds_immunology/41
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentDepartment of Pediatrics
dc.source.pages11429-33


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